Renal failure after hypoperfusion (hypotension, shock, vascular surgery), nephrotoxins (including amphoteracin B), hepatic decompensation, and early allograft rejection results from an increase in renal vascular resistance and a diversion of renal blood flow away from the rapid-transit outer cortical areas. Diuretics (mannitol, ethacrying acid, furosemide) may increase salt and water excretion, but this visible evidence of renal function may not accurately reflect renal perfusion. This study will analyze the renal pharmacology of dopamine and prostaglandin A1. These two agents are direct potent renal vasodilators when given by continuous intravenous infusion, increase salt and water excretion, and may be more effective than diuretics in protecting the kidney during injury and in hastening its recovery. renal blood flow (electromagnetic), flow distribution (microspheres), and autoregulation and clearances of inulin, p- aminohippurate, sodium, potassium, osmoles, and free water will be studied in anesthetized dogs subjected to unilateral renal arterial occlusion with a balloon catheter and intravenous injections of amphoteracin B and gentamicin. Dopamine (2.5 to 50 microgm/km/minute) and prostaglandin A1 (0.25 to 5 microgm/kg/minute) will be infused intravenously consecutively and concurrently. Therapeutic efficacy of dopamine and prostaglandin A1 will be measured in dogs subjected to renal arterial occluson and injection of nephrotoxins (amphoteracin B and gentamicin) and in patients with renal insufficiency secondary to shock, systemic hypoperfusion after cardiac surgery, accelerated hypertension, and nephrotoxic drugs. The ability of dopamine and prostaglandin A1 infusions to hasten renal and peritoneal elimination of poorly-metabolized drugs with a small volume of distribution and weak protein binding will be studied in dogs given barbiturates, salicylates, and imipramine and in patients who have ingested large amounts of similar drugs.